To determine whether the effect of myostatin deletion on adipose tissue size is direct or indirect, we have made a transgenic line of mice that does not have myostatin signaling in fat cells. These mice were created by over-expressing a dominant negative activin type IIB receptor (Acvr2b) under the control of the aP2 promoter. We have characterized the body composition, insulin sensitivity, and resistance to high fat diet of these mice. Mice with adipose tissue-specific inhibition of myostatin signaling have no differences in body weight, body composition, or insulin sensitivity compared to control mice on normal and high-fat diets. These results show that the improved insulin sensitivity, reduction of adipose mass, and resistance to diet-induced obesity seen in myostatin null mice are not due to direct effects of myostatin signaling on adipose tissue.